Journal: STAR Protocols

Article Title: Protocol to reveal the binding partner of secreted housekeeping enzymes in Listeria monocytogenes via in silico prediction to in vivo validation

doi: 10.1016/j.xpro.2024.102839

Figure Lengend Snippet:

Article Snippet: Chloramphenicol, 98% , Thermo Scientific , Cat# AC227920250.

Techniques: Mutagenesis, Plasmid Preparation, Bicinchoninic Acid Protein Assay, Protease Inhibitor, Hot Start PCR, Software, Electroporation, Modification

Journal: BMC Infectious Diseases

Article Title: Cross-sectional study of availability and pharmaceutical quality of antibiotics requested with or without prescription (Over The Counter) in Surabaya, Indonesia

doi: 10.1186/1471-2334-10-203

Figure Lengend Snippet: Characteristics of antibiotic products purchased by simulated clients at medicine outlets in Surabaya, Indonesia

Article Snippet: For content of active ingredient assays of cotrimoxazole, tetracycline, and chloramphenicol the British Pharmacopoeia BP2005 monographs and standards were used [ ], for ciprofloxacin and amoxicillin the United States Pharmacopeia USP 29 [ ].

Techniques:

Journal: BMC Infectious Diseases

Article Title: Cross-sectional study of availability and pharmaceutical quality of antibiotics requested with or without prescription (Over The Counter) in Surabaya, Indonesia

doi: 10.1186/1471-2334-10-203

Figure Lengend Snippet: Antibiotic content of 104 oral samples purchased in medicine outlets in Surabaya, Indonesia

Article Snippet: For content of active ingredient assays of cotrimoxazole, tetracycline, and chloramphenicol the British Pharmacopoeia BP2005 monographs and standards were used [ ], for ciprofloxacin and amoxicillin the United States Pharmacopeia USP 29 [ ].

Techniques:

Journal: BMC Infectious Diseases

Article Title: Cross-sectional study of availability and pharmaceutical quality of antibiotics requested with or without prescription (Over The Counter) in Surabaya, Indonesia

doi: 10.1186/1471-2334-10-203

Figure Lengend Snippet: Retail price comparison of the antibiotics

Article Snippet: For content of active ingredient assays of cotrimoxazole, tetracycline, and chloramphenicol the British Pharmacopoeia BP2005 monographs and standards were used [ ], for ciprofloxacin and amoxicillin the United States Pharmacopeia USP 29 [ ].

Techniques: Comparison

Journal: Antioxidants

Article Title: Polydatin and Nicotinamide Prevent Iron Accumulation and Lipid Peroxidation in Cellular Models of Mitochondrial Diseases

doi: 10.3390/antiox14020215

Figure Lengend Snippet: Superoxide anion production in untreated and treated (+T) control (C1 and C2) and patient (P1, P2, and P3) cells. Cells were treated with polydatin and nicotinamide for seven days. P2 cells treated with 50 µM vitamin E (P2+VitE) served as a negative control. C1 cells were treated with 10 µM chloramphenicol (C1+Chlo) to mimic the mitochondrial protein synthesis deficiency observed in patients’ fibroblasts. ( A ) Representative images of MitoSOX TM staining. Cells were also stained with Mitotracker TM Green FM to visualize the colocalization of both probes. Scale bar: 20 µm. ( B ) Quantification of fluorescence intensity. Data represent the mean ± SD of three independent experiments (at least 30 images were taken from each condition and experiment). Number of biological replicates = 3. **** p < 0.0001 between control and mutant fibroblasts. #### p < 0.0001 between untreated and treated patients’ fibroblasts. aaaa p < 0.0001 between untreated and chloramphenicol-treated C1 cells. bbbb p < 0.0001 between untreated and vitamin E-treated P2 cells. a.u.: arbitrary units. Refer to for comparison between grouped data of controls and patients.

Article Snippet: Anti-iron response protein 1 (IRP1) (sc-166022), anti-ferritin light chain (sc-74513), anti-FPN (sc-518125), anti-Tau (sc-32240), D-galactose (sc-202564), chloramphenicol (sc-3594), and deferiprone (sc-211220) were purchased from Santa Cruz Biotechnology (Dallas, TX, USA).

Techniques: Control, Negative Control, Staining, Fluorescence, Mutagenesis, Comparison

Journal: Antioxidants

Article Title: Polydatin and Nicotinamide Prevent Iron Accumulation and Lipid Peroxidation in Cellular Models of Mitochondrial Diseases

doi: 10.3390/antiox14020215

Figure Lengend Snippet: Intracellular iron accumulation in untreated and treated (+T) control (C1 and C2) and patient (P1, P2, and P3) cells. Cells were treated with polydatin and nicotinamide for seven days. P2 cells were treated with 100 µM deferiprone (P2+Def) to confirm the specificity of Prussian Blue staining for iron. C1 cells were treated with 10 µM chloramphenicol (C1+Chlo) to mimic the mitochondrial protein synthesis deficiency observed in patients’ fibroblasts. ( A ) Representative images of Prussian Blue staining. Scale bar: 20 µm. ( B ) Quantification of iron integrated density. ( C ) Iron content measured by ICP-MS. Data represent the mean ± SD of three independent experiments (at least 30 images were taken from each condition and experiment). Number of biological replicates = 3. **** p < 0.0001 between control and mutant fibroblasts. #### p < 0.0001 between untreated and treated patients’ fibroblasts. aaaa p < 0.0001 between untreated and chloramphenicol-treated C1 cells. bbbb p < 0.0001 between untreated and deferiprone-treated P2 cells. a.u.: arbitrary units. Refer to for comparison between grouped data of controls and patients.

Article Snippet: Anti-iron response protein 1 (IRP1) (sc-166022), anti-ferritin light chain (sc-74513), anti-FPN (sc-518125), anti-Tau (sc-32240), D-galactose (sc-202564), chloramphenicol (sc-3594), and deferiprone (sc-211220) were purchased from Santa Cruz Biotechnology (Dallas, TX, USA).

Techniques: Control, Staining, Mutagenesis, Comparison

Journal: Antioxidants

Article Title: Polydatin and Nicotinamide Prevent Iron Accumulation and Lipid Peroxidation in Cellular Models of Mitochondrial Diseases

doi: 10.3390/antiox14020215

Figure Lengend Snippet: Autofluorescence analysis of untreated and treated (+T) control (C1 and C2) and patient (P1, P2, and P3) cells. Cells were treated with polydatin and nicotinamide for seven days. C1 cells treated with 10 µM chloramphenicol (C1+Chlo) were used to simulate the mitochondrial protein synthesis deficiency observed in patients’ cells. P2 cells treated with 100 µM deferiprone (P2+Def) served as a negative control to confirm the iron-dependence of lipofuscin-like granules. ( A ) Representative images showing GFP and bright field channels of control and mutant GFM1 fibroblasts. Scale bar: 100 µm. ( B ) Autofluorescence spectra of lipofuscin granules with excitation laser at 405 nm. ( C ) Quantification of autofluorescence intensity. Data represent the mean ± SD of three independent experiments (at least 30 images were taken from each condition and experiment). Number of biological replicates = 3. **** p < 0.0001 between control and mutant fibroblasts. #### p < 0.0001 between untreated and treated patients’ cells. aaaa p < 0.0001 between untreated and chloramphenicol-treated C1 fibroblasts. bbbb p < 0.0001 between untreated and deferiprone-treated P2 cells. a.u.: arbitrary units. Refer to for comparison between grouped data of controls and patients.

Article Snippet: Anti-iron response protein 1 (IRP1) (sc-166022), anti-ferritin light chain (sc-74513), anti-FPN (sc-518125), anti-Tau (sc-32240), D-galactose (sc-202564), chloramphenicol (sc-3594), and deferiprone (sc-211220) were purchased from Santa Cruz Biotechnology (Dallas, TX, USA).

Techniques: Control, Negative Control, Mutagenesis, Comparison

Journal: Antioxidants

Article Title: Polydatin and Nicotinamide Prevent Iron Accumulation and Lipid Peroxidation in Cellular Models of Mitochondrial Diseases

doi: 10.3390/antiox14020215

Figure Lengend Snippet: Iron metabolism in untreated and treated (+T) control and patients’ cells. Polydatin and nicotinamide were administered for seven days. ( A ) Immunoblotting analysis of iron metabolism-related proteins in control (C1 and C2) and patient (P1 and P2) cells. ( B ) Band densitometry of Western blot data, referred to actin and normalized to the mean of controls. Data represent the mean ± SD of three independent experiments. Number of biological replicates = 3. **** p < 0.0001 between control and mutant fibroblasts. #### p < 0.0001 between untreated and treated patients’ cells ( C ) Immunoblotting analysis of iron metabolism-related proteins in control (C1 and C3) and patient (P3) cells. ( D ) Band densitometry of Western blot data, referred to actin and normalized to the mean of controls. ( E ) LIP levels determined using a calcein assay. C1 cells treated with 10 µM chloramphenicol (C1+Chlo) were used to mimic the mitochondrial protein synthesis deficiency. C1 cells treated with 100 µM deferiprone (C1+Def) served as a negative control. Data represent the mean ± SD of three independent experiments. Number of biological replicates = 3. **** p < 0.0001 between control and mutant fibroblasts. #### p < 0.0001 between untreated and treated patients’ cells. aaaa p < 0.0001 between untreated and deferiprone-treated C1 fibroblasts. bbbb p < 0.0001 between untreated and chloramphenicol-treated C1 cells. a.u.: arbitrary units. Refer to for comparison between grouped data of controls and patients.

Article Snippet: Anti-iron response protein 1 (IRP1) (sc-166022), anti-ferritin light chain (sc-74513), anti-FPN (sc-518125), anti-Tau (sc-32240), D-galactose (sc-202564), chloramphenicol (sc-3594), and deferiprone (sc-211220) were purchased from Santa Cruz Biotechnology (Dallas, TX, USA).

Techniques: Control, Western Blot, Mutagenesis, Negative Control, Comparison

Journal: Antioxidants

Article Title: Polydatin and Nicotinamide Prevent Iron Accumulation and Lipid Peroxidation in Cellular Models of Mitochondrial Diseases

doi: 10.3390/antiox14020215

Figure Lengend Snippet: Mitochondrial iron levels in untreated and treated (+T) control (C1 and C2) and patient (P1, P2, and P3) cells. Polydatin and nicotinamide were used for seven days. P2 cells treated with 100 µM deferiprone (P2+Def) were used as a negative control. C1 cells treated with 10 µM chloramphenicol (C1+Chlo) were used to simulate mitochondrial protein synthesis deficiency. ( A ) Representative images of mitochondrial iron detected using Mito-FerroGreen. Cells were also stained with Mitotracker TM Deep Red to visualize the colocalization of both probes. Scale bar: 20 µm. ( B ) Quantification of Mito-FerroGreen fluorescence intensity. Data represent the mean ± SD of three independent experiments (at least 30 images were taken from each condition and experiment). Number of biological replicates = 3. **** p < 0.0001 between control and mutant fibroblasts. #### p < 0.0001 between untreated and treated patients’ cells. aaaa p < 0.0001 between untreated and chloramphenicol-treated C1 fibroblasts. bbbb p < 0.0001 between untreated and deferiprone-treated P2 cells. a.u.: arbitrary units. Refer to for comparison between grouped data of controls and patients.

Article Snippet: Anti-iron response protein 1 (IRP1) (sc-166022), anti-ferritin light chain (sc-74513), anti-FPN (sc-518125), anti-Tau (sc-32240), D-galactose (sc-202564), chloramphenicol (sc-3594), and deferiprone (sc-211220) were purchased from Santa Cruz Biotechnology (Dallas, TX, USA).

Techniques: Control, Negative Control, Staining, Fluorescence, Mutagenesis, Comparison

Journal: Antioxidants

Article Title: Polydatin and Nicotinamide Prevent Iron Accumulation and Lipid Peroxidation in Cellular Models of Mitochondrial Diseases

doi: 10.3390/antiox14020215

Figure Lengend Snippet: Lipid peroxidation in untreated and treated (+T) control (C1 and C2) and patient (P1, P2, and P3) cells. Polydatin and nicotinamide were administered for seven days. C1 cells were treated with 10 µM chloramphenicol (C1+Chlo) to mimic the mitochondrial protein synthesis deficiency. C1 cells treated with 500 µM Luperox ® (C1+Lup) served as a positive control for induced lipid peroxidation. P2 cells were treated with 100 µM deferiprone (P2+Def) to confirm the dependence of lipid peroxidation on iron. P2 cells were treated with 50 µM Vitamin E (P2+VitE) as a negative control. ( A ) Representative images of lipid peroxidation using BODIPY ® 581/591 C11 staining. Scale bar: 20 µm. ( B ) Quantification of oxidized fluorescence intensity. ( C ) Immunoblotting analysis of GPX4 in control (C1, C2, and C3) and patient (P1, P2, and P3) cells. ( D ) Band densitometry of Western blot data, referred to actin and normalized to the mean of controls. Data represent the mean ± SD of three independent experiments (at least 30 images were taken for each condition and experiment). **** p < 0.0001 between control and mutant fibroblasts. Number of biological replicates = 3. #### p < 0.0001 between untreated and treated patients’ cells. aaaa p < 0.0001 between untreated and chloramphenicol-treated C1 fibroblasts. bbbb p < 0.0001 between untreated and Luperox ® -treated C1 cells. cccc p < 0.0001 between untreated and deferiprone-treated P2 cells. dddd p < 0.0001 between untreated and Vitamin E-treated P2 cells. a.u.: arbitrary units. Refer to for comparison between grouped data of controls and patients.

Article Snippet: Anti-iron response protein 1 (IRP1) (sc-166022), anti-ferritin light chain (sc-74513), anti-FPN (sc-518125), anti-Tau (sc-32240), D-galactose (sc-202564), chloramphenicol (sc-3594), and deferiprone (sc-211220) were purchased from Santa Cruz Biotechnology (Dallas, TX, USA).

Techniques: Control, Positive Control, Negative Control, Staining, Fluorescence, Western Blot, Mutagenesis, Comparison

Journal: Antioxidants

Article Title: Polydatin and Nicotinamide Prevent Iron Accumulation and Lipid Peroxidation in Cellular Models of Mitochondrial Diseases

doi: 10.3390/antiox14020215

Figure Lengend Snippet: GSH levels in untreated and treated (+T) control (C1 and C2) and patient (P1, P2, and P3) cells. Polydatin and nicotinamide were administered for seven days. C1 cells were treated with 10 µM chloramphenicol (C1+Chlo) to mimic the mitochondrial protein synthesis deficiency. P2 cells were treated with 100 µM deferiprone (P2+Def) to evaluate the dependence of GSH levels on iron. ( A ) Representative images of GSH levels using ThiolTracker TM Violet staining. Scale bar: 20 µm. ( B ) Quantification of fluorescence intensity. Data represent the mean ± SD of three independent experiments (at least 30 images were taken for each condition and experiment). Number of biological replicates = 3. **** p < 0.0001 between control and mutant fibroblasts. #### p < 0.0001 between untreated and treated patients’ cells. aaaa p < 0.0001 between untreated and chloramphenicol-treated C1 fibroblasts. bbbb p < 0.0001 between untreated and deferiprone-treated P2 cells. a.u.: arbitrary units. Refer to for comparison between grouped data of controls and patients.

Article Snippet: Anti-iron response protein 1 (IRP1) (sc-166022), anti-ferritin light chain (sc-74513), anti-FPN (sc-518125), anti-Tau (sc-32240), D-galactose (sc-202564), chloramphenicol (sc-3594), and deferiprone (sc-211220) were purchased from Santa Cruz Biotechnology (Dallas, TX, USA).

Techniques: Control, Staining, Fluorescence, Mutagenesis, Comparison

Journal: Antioxidants

Article Title: Polydatin and Nicotinamide Prevent Iron Accumulation and Lipid Peroxidation in Cellular Models of Mitochondrial Diseases

doi: 10.3390/antiox14020215

Figure Lengend Snippet: Mitochondrial lipid peroxidation in untreated and treated (+T) control (C1 and C2) and patient (P1, P2, and P3) cells. Cells were treated with polydatin and nicotinamide for seven days. C1 cells were treated with 10 µM chloramphenicol (C1+Chlo) to simulate the mitochondrial protein synthesis failure of patients’ fibroblasts. P2 cells were treated with 100 µM deferiprone (P2+Def) as a negative control. ( A ) Representative images of mitochondrial lipid peroxidation using MitoPeDPP ® staining. Cells were also stained with Mitotracker TM Deep Red FM to visualize the mitochondrial network. Nuclei were visualized by DAPI staining. Scale bar: 20 µm. ( B ) Quantification of fluorescence intensity. Data represent the mean ± SD of three independent experiments (at least 30 images were taken for each condition and experiment). Number of biological replicates = 3. **** p < 0.0001 between control and mutant fibroblasts. #### p < 0.0001 between untreated and treated patients’ cells. aaaa p < 0.0001 between untreated and chloramphenicol-treated C1 fibroblasts. bbbb p < 0.0001 between untreated and deferiprone-treated P2 cells. a.u.: arbitrary units. Refer to for comparison between grouped data of controls and patients.

Article Snippet: Anti-iron response protein 1 (IRP1) (sc-166022), anti-ferritin light chain (sc-74513), anti-FPN (sc-518125), anti-Tau (sc-32240), D-galactose (sc-202564), chloramphenicol (sc-3594), and deferiprone (sc-211220) were purchased from Santa Cruz Biotechnology (Dallas, TX, USA).

Techniques: Control, Negative Control, Staining, Fluorescence, Mutagenesis, Comparison

Journal: Antioxidants

Article Title: Polydatin and Nicotinamide Prevent Iron Accumulation and Lipid Peroxidation in Cellular Models of Mitochondrial Diseases

doi: 10.3390/antiox14020215

Figure Lengend Snippet: Ferroptosis sensitivity in untreated and treated (+T) control (C1 and C2) and patient (P1, P2, and P3) fibroblasts. Polydatin and nicotinamide were used for seven days. C1 cells treated with 10 µM chloramphenicol (C1+Chlo) were used to mimic the patients’ pathogenic variant. P2 cells treated with 100 µM deferiprone (P2+Def) were used as a negative control. ( A ) Representative images of dead cells staining with PI over the course of 25 h after the supplementation with 5 µM erastin. Scale bar: 20 µm. ( B ) Quantification of PI positive cells over the period of 25 h. ( C ) Quantification of PI positive cells at 25 h after the addition of erastin. Data represent the mean ± SD of three separate experiments (at least 30 images were taken for each condition and experiment). Number of biological replicates = 3. **** p < 0.0001 between control and mutant fibroblasts. #### p < 0.0001 between untreated and treated patients’ cells. aaaa p < 0.0001 between untreated and chloramphenicol-treated C1 fibroblasts. bbbb p < 0.0001 between untreated and deferiprone-treated P2 cells. Refer to for comparison between grouped data of controls and patients.

Article Snippet: Anti-iron response protein 1 (IRP1) (sc-166022), anti-ferritin light chain (sc-74513), anti-FPN (sc-518125), anti-Tau (sc-32240), D-galactose (sc-202564), chloramphenicol (sc-3594), and deferiprone (sc-211220) were purchased from Santa Cruz Biotechnology (Dallas, TX, USA).

Techniques: Control, Variant Assay, Negative Control, Staining, Mutagenesis, Comparison

Journal: bioRxiv

Article Title: Mitochondrial protein translation is a heightened dependence and therapeutic vulnerability of chemo-refractory triple negative breast cancer

doi: 10.64898/2026.03.23.712647

Figure Lengend Snippet: MDA-MB-231 cells were treated with vehicle (VEH) or tigecycline (TIG 8 µM) for two days. (A) IC 50 dilution curve, (B) western blotting of whole cell lysates probing for ETC proteins, (C) mtDNA:nDNA ratio, and (D) qRT-PCR analysis of mitochondrial gene expression. Expression of mtDNA-encoded genes was normalized to TUBB . (E) Coomassie staining of a native gel to assess SC formation, and SDS-PAGE western blot of mitochondrial and cytoplasm fractions. (F) Blue native-PAGE immunoblotting for complex III: UQCRC2 and measurement of SC bands compared to total UQCRC2 by densitometry. (G) Seahorse MitoStress Tests showing a representative biological replicate for the tombstone plot and all biological replicates in the bar graphs. OCR and ECAR values were normalized to viable cell counts. Data are shown as mean ±SEM, and individual data points represent biological replicates. Significant comparisons are indicated; *p < 0.05, **p < 0.01, ***p < 0.001, ****p<0.0001 by unpaired t-test.

Article Snippet: Tigecycline (Selleck Chemicals S1403) and chloramphenicol (Selleck Chemicals S1677) were prepared fresh in DMSO.

Techniques: Western Blot, Quantitative RT-PCR, Gene Expression, Expressing, Staining, SDS Page, Blue Native PAGE